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L.acidophilus participates in intestinal inflammation induced by PM2.5 through affecting the Treg/Th17 balance
Jie Xu1, Jing Wang2, Yuefeng He1
1Yunnan Provincial Key Laboratory of Public Health and Biosafety & School of Public Health, Kunming Medical University, Kunming 650500, China.
Abstract:
Particulate matter with aerodynamic diameters of ≤2.5 μm (PM2.5) is associated with multiple organ damage, among which the influence of PM2.5 on the gastrointestinal system has been a recent focus of attention. In this study, four different types of PM2.5 exposure models are established to determine the occurrence of PM2.5 induced intestinal inflammation. In view of the abnormal expression of lymphocytes detected in the model and the well-known fact that the intestine is the largest immune organ, we focused on the intestinal immune system. A combined regulatory T cell (Treg) transplantation experiment demonstrated that PM2.5 induced intestinal inflammation by affecting the imbalance of regulatory T cell/T helper cell 17 (Treg/Th17). Since the intestine has the highest microbial content, and the results of the 16S rDNA third-generation sequencing analysis further revealed that the abundance of Lactobacillus_acidophilus (L.acidophilus) decreased significantly after PM2.5 exposure. The following mechanism study confirmed that L.acidophilus participated in an imbalance of Treg/Th17. Moreover, L.acidophilus supplementation successfully alleviated intestinal inflammation by regulated regulating the balance of Treg/Th17 under the background of PM2.5 exposure. Hence, this is a potential method to protect against intestinal inflammation induced by PM2.5.
Insights
Particulate matter (PM2.5) exposure causes intestinal inflammation by disrupting the Treg/Th17 balance and reducing Lactobacillus acidophilus. Supplementing L. acidophilus can protect against this inflammation.
Area of Science:
- Environmental Health
- Gastroenterology
- Immunology
Background:
- Particulate matter (PM2.5) is linked to multi-organ damage, with growing interest in its gastrointestinal effects.
- The intestine, a major immune organ with high microbial content, is susceptible to PM2.5-induced inflammation.
Purpose of the Study:
- To investigate the mechanisms of PM2.5-induced intestinal inflammation.
- To explore the role of the gut immune system and microbiota in PM2.5 exposure.
Main Methods:
- Established four PM2.5 exposure models in rodents.
- Conducted regulatory T cell (Treg) transplantation experiments.
- Utilized 16S rDNA third-generation sequencing for microbial analysis.
- Performed mechanistic studies on Lactobacillus acidophilus (L. acidophilus) and Treg/Th17 balance.
Main Results:
- PM2.5 exposure induced intestinal inflammation by creating an imbalance between regulatory T cells (Tregs) and T helper 17 cells (Th17).
- PM2.5 significantly decreased the abundance of L. acidophilus in the gut.
- L. acidophilus was confirmed to be involved in the Treg/Th17 imbalance.
- Supplementation with L. acidophilus alleviated PM2.5-induced intestinal inflammation by restoring Treg/Th17 balance.
Conclusions:
- PM2.5 exposure disrupts the intestinal immune homeostasis, specifically the Treg/Th17 balance, contributing to inflammation.
- L. acidophilus plays a crucial role in mitigating PM2.5-induced gut inflammation.
- L. acidophilus supplementation presents a potential therapeutic strategy against PM2.5-related intestinal damage.
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